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Leucocytosis. Leucopenia. Leucosis
 

Prepared By MD, PhD. Marta R. Gerasymchuk, pathophysiology department of Ivano-Frankivsk National Medical University, Ukraine

Prepared By MD, PhD. Marta R. Gerasymchuk, pathophysiology department of Ivano-Frankivsk National Medical University, Ukraine
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  • ALL blasts look the same on routine stains, whether they are myeloblasts, lymphoblasts, monoblasts, etc. A blast is a blast! Please remember you have all been conditioned to think a NUCLEOLUS is darker than the rest of the NUCLEUS, as it is on H&E, but in the usual stains we stain bone marrow smears or peripheral smears with, the nucleoli are LIGHTER!!!
  • MYELOPEROXIDASE stains are often use to identify cells believed to be of MYELOID origin, such as blastic looking cells, but you cannot really tell for sure on Wright’s or Giemsa stains.
  • TOXIC GRANULES are EXAGGERATIONS of the marrow’s normal granularity, DOHLE bodies are fragments of remaining dilated rough ER. Neutrophilia can be viewed as a NONSPECIFIC index of acute infection, especially bacterial, but also tissue necrosis.
  • Not only are basophils RARE to find normally, but pure “basophilia” is also VERY rare.
  • Why would monocytosis be linked to granulomatous diseases? Answer: Monocytes are macrophages in circulation, and granulomatous diseaseas are macrophage diseases. Is it surprising that many classical granulomatous diseases are also characterized by monocytosis, because macrophages are the CHIEF cells of granulomas? Answer: NO, not surprizing, it would be logical even!
  • Would it be a fair statement to say that whereas, neutrophilia is characterized by bacterial infections, lymphocytosis can be an index of many viral infections? Answer: Yes, it is fair, but there are many exceptions.
  • The most life saving thing you can learn today is how to recognize a blast! HUGE NUCLEUS NUCLEOLI (stain LIGHTER not DARKER than the rest of the nucleus on Wright stain), How many nucleoli does that one blast cell have? Answer: 3 NO cytoplasmic differentiation
  • Ataxia-Telangiectasia is characterised by: Early-onset progressive  cerebellar ataxia  (difficulty with control of movement) Ocular apraxia (difficulty following objects across visual field) Telangiectasias  of the eyes and skin Immunodeficiency , low immunoglobulin concentrations Chromosomal  instability Hyper-sensitivity to  ionizing radiation Increased incidence of malignancies (primarily hematologic). Raised  alpha-fetoprotein  levels. [4] Absent thymic shadow on X-ray. Ovarian dysgenesis
  • Acute promyelocytic leukemia, remember promyelocytes have BOTH nucleoli AND nonspecific granules, true BLASTS do NOT have granules. Do you remember that M3 has a high degree of association with DIC?
  • You can usually diagnose CLL simply from a CBC printout, but should verify the cells visually.
  • Many cells from CLL have a “smudge” or “basket” appearance
  • Note the “lytic” lesions. Often the term “punched out” is used also.

Leucocytosis. Leucopenia. Leucosis Leucocytosis. Leucopenia. Leucosis Presentation Transcript

  • By MD, PhD. Marta R. Gerasymchuk16th January 2013
  • Plan of the lectur e1. Leucopoesis.2. Leucocytosis. Deffinition. Classification.3. Pathogenesis of leucocytosis.4. Leucopenias. Deffinition.Classification.5. Pathogenesis of leucopenias.6. Agranulocytosis.7. Leucemias. Deffinition. Classification. Pathogenesis. Clinical signts.8. Treatment of leucemias.9. Leucemoid reactions.
  • Actuality of the lecture Leucocytosis are considered as a reaction hematopoietic system due toaction of physiological and pathological irritations. Leucocytosis is apathological symptom of many diseases. In a basis of leucocytosis laypathophysiological mechanisms connected with proliferation, maturationgoing out of leucocytes and their flow into vessels and redestribution.Different kinds of leucocytosis may be the additional criteri for establishthe diagnosis. Eosinophilia, for example, is characterized for allergyreactions, neutrophile leucocytosis - for acute inflamation processes. Leucopenia may depend upon oppressive influence of some toxines onthe maturation and outflow of leucocytes from the bone-marrow. Oftenthese phenomenas are observed during the infectious diseases. Theyhave significanse for the differential diagnostic. If for the disease ischaracterised leucocytosis, the availability of leucopenia testifies ondepression of hemopoietic system. It is regarded as a criteri weakenes ofreactivity of the body on action of pathological factors.Directness andcharacter of changes of white blood cells due to various diseases -significant for the diagnosis and control of the treatment.
  • WBC’s
  • PMN-Polymorphonuclear Neutrophil Leucocytes. 60-70% WBC Appearance: pink granules in cytoplasm, nucleus has 3-4 lobes Function:♦ Margination♦ Rolling♦ Adhesion♦ Transmigration (Diapedesis)♦ Chemotaxis♦ Phagocytosis: Recognition, Engulfment, Killing (digestion)♦Equilibrium with splenic pool Azurophilic (1°) granules are "lysosomes of PMNs", occur in all leukocytes DÖHLE BODIES and TOXIC GRANULES are often seen with NEUTROPHILIA Accompanied by a “LEFT” shift
  • PELGER-HUET ANOMALY Genetic Sometimes ACQUIRED (Pseudo-PELGER-HUET) All neutrophils look like BANDS NOT serious, mostly a cute incidental finding
  • CHEDIAK-HIGASHI SYNDROME Also genetic Abnormal LARGE irregular neutrophil granules Impaired lysosomal digestion of bacteria Associated with pigment and bleeding disorders CAN be serious, especially in kids
  • Eosinophil (Eos)  Bilobed nucleus  2-4% of WBC  Recruited to sites of inflammation  Function: Involved in allergy, parasitic infections  Contains: eosinophilic granules  Granules contain: major basic protein  Terminally differentiatedAzurophilic granuels
  • Basophil • Circulating form of mast cells • Terminally differentiated • <1% WBC (< 1 x 10*9/L) • Contains: basophilic granules • Granules contain: histamine and heparin • IgE receptors • Involved in allergy
  • Monocyte / Macrophage Monocyte • 3-8% WBC • Circulating form (precursor) of tissue macrophages • Recruited to sites of inflammation Macr opha ges • Phagocytosis, bacterial killing, antigen presentation • Peritoneal cavity: peritoneal macrophages • Lung: alveolar macrophages • Spleen: splenic macrophages • Liver: Kupffer cells
  • BT Lymphocyte •Appearance: small (same size as RBCs), little visible cytoplasm •NO specific granules B • 20-25% of WBC •T cells: CMI (for viral infections) T • B cells: humoral (antibody) • Natural Killer Cells
  • Leukocytosis Primary SecondaryAbsolute Relative Absolute RelativeStimulation of Redistribution 1. Stimulation of 1.Hemoconcentraleukopoiesis of leukocytes leukopoiesis tional- in vascular bed 2. Increase ofLeukocytosis - alimentary, leukocytes transport 2.Redistributionalof pregnant - emotional, from bone marrow(5-6 mounts - myogenic, 3. Increase ofof pregnancy) - static tumoral type of leukopoiesis during leukosis
  • Leukocytosis
  • 4000-9000 Leukocytosis• Neutrophylia – Acute bacterial infection, sterile inflammationEosinophylia – Allergy (allergic rhinitis, other hypersensitivity reactions,including drug reactions) , parasites (ascaris, hookworm, strongiloides), certain skin diseases, cancer (adenocarcinoma)• Basophilia – rare (leukemia)• Monocytosis – chronic infections, bacterial endocarditis, rickettsiosis, malaria, collagen vascular disorders, inflammatory bowel diseases• Lymphocytosis – some viral infections
  • Leukopenias Primary (hereditary) Secondary (Acquired)1. Deficit of maturity factors Absolute Relative- constant hereditaryneutropenia 1. Inhibition of 1. Redistributional leukopoiesis e.g. shock, civere-periodic hereditary 2. Increase of muscular work etc.neutropenia leukodieresis 2. Hemodilutional2. Deficit of myeloperoxidase, 3. Increase of e.g. blood plasma,G-6-PhDG leukocyte loss transfusion of blood 4. Decrease of- hereditary monocytopenia substitutes, hydremia leukocyte emigrationwith phagocytic insufficiency etc. from bone morrowdeficit (disease of Chediak-Higashi)
  • Causes of Neutropenia Cause MechanismAccelerated removal (e.g., inflammation and Removal of neutrophils from the circulation exceeds infection) productionDrug-induced granulocytopenia Defective production Cytotoxic drugs used in cancer therapy • Predictable damage to precursor cells, usually dose dependent Phenothiazine, thiouracil, • Idiosyncratic depression of bone marrow chloramphenicol, phenylbutazone, and others function Hydantoinates, primidone, and others • Intramedullary destruction of granulocytes Immune destruction • Immunologic mechanisms with cytolysis or Aminopyrine and others leukoagglutinationPeriodic or cyclic neutropenia (occurs during infancy Unknown and later)Neoplasms involving bone marrow (e.g., leukemias Overgrowth of neoplastic cells, which crowd out and lymphomas) granulopoietic precursorsIdiopathic neutropenia that occurs in the absence of Autoimmune reaction other disease or provoking influenceFelty’s syndrome Intrasplenic destruction of neutrophils
  • AGRANULOCYTOSIS Myelotoxic Immune1. Cytolytic influence, e.g. 1. Autoimmune e.g. lupus ionizing radiation etc. erythematosus,2. Antimetabolic influence rheumatoid arthritis e.g. cytostatics etc. 2. Heteroimmune
  • WBC Neoplastic disorders : Leukemias Bone marrow, blood, blast cells  Acute / Chronic & Myeloid / Lymphoid  AML / ALL & CML / CLL Lymphomas – Lymph nodes, tumor  Hodgkins -  Non-Hodgkins. Myeloma  High grade & Low grade Premalignant conditions:  Myeloproliferative syndromes (MPS)  Myelodysplastic syndromes (MDS)
  • Mechanisms of bone mar r ow neoplasia Blast cells (malignant) overpopulate the bone marrow and replace the normal cells causing bone destruction and/or blood or lymphoid cell deficiencies. Malignant cells or their descendents may appear in the peripheral blood (leukemia), in extramedullary sites such as the spleen and liver (hepatosplenomegaly) and in lymph nodes (lymphadenopathy). Bone marrow malignancy may be accompanied by myelofibrosis (the extensive deposition of collagen by non- neoplastic fibroblasts). Types of bone marrow neoplasia: Malignant transformation of hematopoietic and lymphoid cell precursors may occur at any point in their maturation. Malignant cells are classified as myeloid, lymphoid or plasmacytic. The characteristic behavior of particular malignant stem cells determines the presentation of the disease.
  • Types of bone marrow neoplasia1. Myeloproliferative disorders: Characterized by the malignant transformation of developmentally pluripotent myeloid stem cells and their linage- restricted descendants.2. Myelodysplastic syndromes: Characterized by ineffective hematopoiesis and pancytopenia.3. Leukemia: Characterized by the appearance of neoplastic WBCs in the peripheral circulation.4. Plasma cell disorders: Characterized by the monoclonal proliferation of neoplastic plasma cells and plasmacytoid lymphocytes usually in the bone marrow
  • Neoplastic WBC Disorders: No Benign Neoplasms – All are considered malignant or premalignant. Cells flood blood stream – Leukemia. Arise in marrow(myeloid/lymphoid) or Lymphnode (lymphoid), then spread to blood & other organs  Malignant  Premalignant:  Leukemias  Myeloproliferative  Lymphomas  Myelodysplastic Sy.
  • Myeloproliferative DisordersThese disorders include:• polycythemia rubra vera (proliferation of RBC precursors),• essential thrombocytemia (proliferation of platelet precursors)• chronic myelocytic leukemia (proliferation of neutrophil precursors) and• myelofibrosis (proliferation of fibroblasts).These entities are interrelated and may transform one into another or into acute myeloblastic leukemia (AML). Features common to all myeloproliferative disorders:1. Peak incidence in 40-70 years of age2. Marrow hypercellularity, except myelofibrosis which is dominated by fibrosis3. Splenomegaly due to extramedullary hematopoiesis4. Peripheral blood abnormalities and hyperviscosity, except for myelofibrosis
  • MPS: Classification
  • MPS - P. Rubra Vera (PV)
  • Myelodysplastic syndromes Myelodysplastic syndromes (MDS, formerly known as "preleukemia") are a diverse collection of hematological conditions united by ineffective production of blood cells and varying risks of transformation to acute myelogenous leukemia (AML). Anemia requiring chronic blood transfusion is frequently present. Myelodysplastic syndromes (MDS) are bone marrow stem cell disorders resulting in disorderly and ineffective hematopoiesis manifested by irreversible quantitative and qualitative defects in hematopoietic cells. In a majority of cases, the course of disease is chronic with gradually worsening cytopenias due to progressive bone marrow failure. Approximately one-third of patients with MDS progress to AML within months to a few years. The median age at diagnosis of a MDS is between 60 and 75 years; a few patients are less than 50; MDS are rare in children. Males are slightly more commonly affected than females. Signs and symptoms are nonspecific and generally related to the blood cytopenias (anemia, neutropenia, thrombocytopenia). A significant proportion of the morbidity and mortality attributable to MDS results not from transformation to AML but rather from the cytopenias seen in all MDS patients. Anemia is most common and responds to transfusion, patients often suffer from iron overload. The two most serious complications in MDS patients resulting from their cytopenias are bleeding (due to lack of platelets) or infection (due to lack of white blood cells).
  • Myelodysplastic Syndromes: Excess proliferation in marrow. But functional & Structural abnormality Ineffective Myelopoiesis. Peripheral pancytopenia. Also known as Refractory Anemia’s Not responding to hematenics.
  • MPS : E.T. Bleeding
  • LEUKEMIAS ■ Leukemias are malignant neoplasms arising from the transformation of a single blood cell line derived from hematopoietic stem cells. ■ The leukemias are classified as acute and chronic lymphocytic (lymphocytes) or myelogenous (granulocytes, monocytes) leukemias, according to their cell lineage. ■ Because leukemic cells are immature and poorly differentiated, they proliferate rapidly and have a long life span; they do not function normally; they interfere with the maturation of normal blood cells; and they circulate in the bloodstream, cross the bloodbrain barrier, and infiltrate many body organs.
  • Leukemia Classification Acute Leukemias:  Acute Myeloid Leukemia - AML  AML M0, M1, M2, M3, M4, M5, M6 & M7  Acute Lymphoid Leukemia - ALL  ALL - L1, L2 & L3 - maturity Chronic Leukemias:  Chronic Myeloid Leukemia- CML  Chronic Lymphoid Leukemia - CLL
  • Leukemia –ClinicalFeatures Anemia (low RBC) Fever - Infections (low WBC) Bleeding tendency (low PLT) Tender bones, lymphadenopathy, spleenomegaly etc. (Leukemic infiltration) Intoxication Autosensitization (esp. lymphogenic L.)
  • AML-M5 - Gum Hypertrophy:
  • AML- Marked Purpura:
  • ALL:Cervical Lymphadenopathy
  • LEUKEMIASAcute or Chronic Myeloid or Lymphocytic Childhood or Adult All involve marrow All ACUTE leukemias suppress normal hematopoesis, i.e., have anemia, thrombocytopenia Most have chromosomal aberrations Some can respond DRASTICALLY to chemo, most notably ALL in children, even be cured!!!!
  • BLAST
  • WHITE CELL NEOPLASMS Leuk/Lymph Many have chromosomal translocations Can arise in inherited and/or genetic diseases:  Downs Syndrome (Trisomy 21)  Fanconi’s anemia (hereditary aplastic anemia)  Ataxia telangiectasia May have a STRONG viral relationship:  HTLV-1 (lymphoid tumors)  EBV (Burkitt Lymphoma)  Human Herpesvirus-8 (B-Cell Lymphomas) (also KS)
  • WHITE CELL NEOPLASMS Leuk/Lymph Can be caused by H. Pylori (gastric B- Cell lymphomas) Can follow celiac disease (gluten sensitive enteropathy T-Cell lymphomas) Are common in HIV, B-Cell lymphomas, CNS lymphomas
  • Types of Leukemias1. Acute Lymphoblastic leukemia (ALL) ~30% of all leukemias, the most common among children under 5 years old. The marrow contains more than 30% lymphoblasts. The prognosis is inversely proportional to age.2. Acute myelogenous leukemia (AML) ~80% of acute leukemias in adults. Marrow has >20% myeloblasts. Overall prognosis is poor with relapse after chemotherapy and most do not survive more than 5 years after diagnosis. Two forms; acute denovo AML or as an end-stage of CML and myelofibrosis. ALL AML
  • Types of Leukemias 3. Chronic lymphocytic leukemia (CLL) Peak incidence is in elderly males >60years old. Bone marrow has >40% lymphoid cells, peripheral blood has >15 X10↑6. Neoplastic cells resemble B-lymphocytes. CLL has an indolent course over 7- 10 years, it responds poorly to chemotherapy. It is closely related to small cell lymphoma and lymphadenopathy is common. 4. Chronic myelogenous leukemias (CML) Peak incidence is ~60years old. Symptoms are related to loss of normal marrow functioning; anemia, bleeding & infection. Peripheral WBC counts in the 20-50,000 range with large component of myeloid precursors. Frequently terminates in a “blast” crisis with peripheral WBCs of >100,000 with immature myeloid cells. Prognosis is poor despite chemotherapy.
  • ALL-Acute Lymphocytic Leuk. Common in Children. FAB classification L1, L2 & L3 B cell, T cell & histiocytic types. CD10 +ve, Pre B cell type common. Lymphadenopathy, bleeding tendency Moderate Hepatosplenomegaly
  • ALL-L1
  • ALL-L2
  • ALL-L3
  • AML-Acute Myeloid Leuk. Malignancy of myeloid progenitor cells. Adults common Hepatosplenomegaly moderate No significant lymphadenopathy Bleeding tendency Gum bleeding common in M5/M4 FAB classification - M0 to M7.
  • AML-Acute Myeloid Leuk.► M0 - AML No maturation (<3% Peroxidase +ve)► M1 - AML Min.Maturation(>3% Peroxidase +ve)► M2 - AML With full maturation► M3 - A.Promyelocytic leukemia► M4 - A.Myelomonocytic leukemia► M5 - A.Monocytic L(a-Monocytic, b-M.blastic)► M6 - A. Erythroleukemia► M7 - A. Megakaryocytic leukemia.
  • AML-M0 - Undifferentiated:
  • AML-M1 - without maturation
  • AML-M2 - with maturation
  • AML-M3 - Auer Rods
  • M3 Acute promyelocytic leukemia, remember promyelocytes have BOTH nucleoli AND nonspecific granules, true BLASTS do NOT have granules.
  • AML-M3 - Promyelocytic
  • AML-M4 - Myelomonocytic
  • AML-M5b - Monoblastic Leuk
  • AML-M6 :Erythroleukemia
  • AML-M7 : Megakaryocytic
  • Chronic Myeloid Leukemia• Middle age 40-60y• Philadelphia chromosome, t(9:22)• Leucocytosis (>50x109/L), abnormal cells• Marked splenomegaly• Anemia, Bleeding• Hypermetabolism,• Hyperuricemia- gout, renal impairment.
  • Chronic Myelogenous Leukemia, BCR-ABL1+ • Chronic myelogenous leukemia presenting in blast phase including lymph node involvement. • A, Peripheral blood smear with leukocytosis, massive left shift with “myelocyte bulge” and 7% blasts (Wright- Giemsa). • B, Inguinal lymph node with sheets of blasts (H&E). • C, Blasts positive for CD3 antigen. Contributed by N. Vajpayee and colleagues.
  • Chronic Myelomonocytic Leukemia • Circulating promonocytes are present (A and B) in a sample from a patient with chronic myelomonocyti c leukemia (A and B), blood sample.
  • C.L.L.• Unexplained sustained (months) lymph count of > 4000/mm3 is CLL, usually picked up on CBC• M>F• Lymphs look normal and are NOT blasts• No need for marrow exam for dx, but progressive involvement of marrow, nodes, and other organs is the usual biologic behavior• Liver can be involved portally or sinusoidally• Translocations RARE, but trisomies and deletions common
  • C.L.L.
  • C.L.L.• HYPO-gammaglobulinemia• 15% have antibodies against RBC’s or PLATS• CANNOT be classified as separate from lymphomas
  • LymphomasNeoplasms of lymphoid cells may be divided into two major groups:• Non-Hodgkin’s lymphoma ~70%• Hodgkins lymphoma ~30%Predisposing factors1. Oncogenes, both lymphomas & leukemias may share the same oncogenes.2. Radiation increases the risk of lymphomas particularly radiation therapy for neoplastic disorders.3. Environmental factors, Burkitt lymphoma is related to EBV infection.4. Immunodeficiency states (congenital or acquired) are associated with an increased incidence of lymphomas; HIV is associated with CNS lymphoma.
  • (MALIGNANT) LYMPHOMAS► Terms in historic classifications:  Diffuse/Follicular, Small/Large, Cleaved/Non- cleaved  Hodgkins (REED-STERNBERG CELL) /NON- Hodgkins  Lukes, Rappaport, etc.  Working Formulation, WHO, NIH, FAB, Intl., etc. B T  PRECURSOR (less mature looking)
  • Hodgkins Lymphoma: Hodgkin’s disease is a group of cancers characterized by Reed-Sternberg cells that begins as a malignancy in a single lymph node and then spreads to contiguous lymph nodes Lymphadenopathy, painless, firm Pel-Ebstein fever, Eosinophilia, Reed-Sternberg cells - B lymphocytes Histological Types: – Lymphocyte predominant. – Nodular Sclerosis. – Mixed cellularity. – Lymphocyte depleted.
  • Non-Hodgkins Lymphoma: Non-Hodgkin’s lymphomas represent a group of heterogeneous lymphocytic cancers that are multicentric in origin and spread to various tissues throughout the body, including the bone marrow. According to cell type According to Clinical grade  T cell NHL •Low grade NHL  B cell NHL •High grade NHL •Intermediate grade NHL  Miscellaneous NHL Ex: Lennert’s lymphoma is a low grade T cell NHL. Burkitt’s lymphoma is a high grade B cell NHL
  • Non-Hodgkin lymphomas Burkitt lymphoma is a rapidly growing B-cell lymphoma affecting children and adults. It is related to EB virus infection. Solid tumors are often located in extranodal tissue. Response to chemotherapy is inversely related to age.
  • Hodgkin’s disease comprise several closely related neoplastic lymph node disorders that resemble lymphomaAreas of involvement: This usually involves a neoplastic process in contiguous lymph nodes usually in the neck and mediastinum. Extranodal involvement and disease above and below the diaphragm portend poor prognosis.
  • Clinical Differences Between Hodgkin and Non-Hodgkin Lymphomas Hodgkin Lymphoma Non-Hodgkin Lymphoma More often localized to a More frequent single axial group of involvement of nodes (cervical, multiple peripheral mediastinal, para-aortic) nodes Orderly spread by Noncontiguous spread contiguity Mesenteric nodes and Waldeyer ring and Waldeyer ring rarely mesenteric nodes involved commonly involved Extranodal involvement Extranodal uncommon involvement common
  • Leukemoid Reactionan excessive leukocytic responseleukocytosis of 50 x109/L or higherwith shift to the leftorlower counts with considerable numbersof immature granulocytesquantitative or qualitative changes inlymphocytes or monocytes
  • Leukemoid Reaction hemolysisparasite hemorrhage malignancy Hodgkin disease myelofibrosis eosinophilic neutrophilic TB burns lymphocytic eclampsia infectious lymphocytosis pertussis TB
  • Plasma cell disor der s Main types  Multiple myeloma  Waldenstrom macroglobulinemia: A malignancy of plasmacytoid lymphocytes that secrete IgM resulting in a hyperviscosity syndrome with renal, retinal and cerebral ischemia as a result of microvascular occlusion.  Monoclonal gammopathy of unknown significance: often diagnosed in asymptomatic elderly patients. It is present in ~1% of patients over 60 years old and 3% of patients over 70. There is a 1% risk of developing multiple myeloma. Clinical features  Tend to occur in those >45 years old.  Neoplastic plasma cells produce a monoclonal immunoglobulin component that can be identified by serum electrophoresis  Deposition of light chain immunoglobulin may form amyloid deposits in the kidneys, vessels and other organs.
  • Multiple Myeloma• A neoplasm of mature plasma cells that respond poorly to chemotherapy and usually survive ~3 years after diagnosis. Renal damage due to protein deposition is the most common cause of death. Infection, systemic amyloidosis, anemia, hyperviscosity and metabolic disorders contribute to the poor outcome.
  • Multiple MyelomaClinical Presentation: - Pts present in their middle fifties or older (60-70 yr)- Constitutional symptoms, anemia, thrombocytopenia, and renal failure;- Approx 80% of pts have chief complaint of bone pain w/ diffuse bone tenderness, particularly over the sternum and pelvis.- Pathological fracture of spine or femur may be heralding event;- Symptoms range in duration from as short as few wks to as long as 2 yrs.
  •  Neoplastic cells secrete a monoclonal immunoglobulin: IgG 60%, IgA 20% and IgD, IgE or the heavy or light chain 20%. Normal immunoglobulins are suppressed increasing the risk of infection. Multiple bone lesions are composed of nests of neoplastic cells and appear as “punch” lesions in bones. Bony lesions may cause symptomatic hypercalcemia, metastatic calcification also occurs. Excess immunoglobulin may be deposited in peripheral tissue forming amyloid. They may be secreted in the urine as Bence- Jones proteins, occasionally proteins obstruct renal tubules resulting in renal failure.
  • SUMMARY
  •  Literature Anatoliy V. Kubyshkin – General and clinical pathophysiology / Edited by Vinnytsia: Nova Knuha Publishers – 2011. – p.286–287, 322–333. Handbook of general and Clinical Pathophysiology / Edited by prof.A.V.Kubyshkin. – CSMU. – 2005. – p.142–144. Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. – p.125– 133, 145–153. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – p. 297-311. 1. General and clinical pathophysiology. Workbook for medical students and practitioners. – Odessa. – 2001. 2. J.B.Walter I.C.Talbot General pathology. Seventh edition. – 1996. 3. Stephen J. McPhee, William F. Ganong. Pathophysiology of Disease, 5th edition. – 2006. 4. Robbins and Cotran Pathologic Basis of Disease 7th edition./ Kumar, Abbas, Fauto. – 2006. 5. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – p. 301-308.
  • Dexter star Michael C. Hallfights against Hodgkin’s Lymphoma